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Pregestational diabetes increases fetoplacental vascular resistance in rats

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F18%3A10375348" target="_blank" >RIV/00216208:11130/18:10375348 - isvavai.cz</a>

  • Result on the web

    <a href="https://doi.org/10.1016/j.placenta.2018.01.008" target="_blank" >https://doi.org/10.1016/j.placenta.2018.01.008</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.placenta.2018.01.008" target="_blank" >10.1016/j.placenta.2018.01.008</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Pregestational diabetes increases fetoplacental vascular resistance in rats

  • Original language description

    Introduction: Diabetes is a well-known risk factor in pregnancy. Because maternal diabetes involves oxidative stress that is also induced by chronic hypoxia and can alter vascular function, we sought to determine the effects of chronic maternal hyperglycemia on the fetoplacental vasculature in rats and to compare it with the effects of chronic hypoxia. Methods: Diabetes was induced in female rats by a streptozotocin injection at a neonatal age. When these animals reached adulthood, their hyperglycemia was confirmed and they were inseminated. Half of them were exposed to hypoxia (10% O-2) for the last week before the delivery. One day before the expected date of delivery, one of their placentae was isolated and perfused. Results: Fetoplacental vascular resistance was increased equally by experimental diabetes, chronic hypoxia, and their combination. Fetoplacental perfusion pressure-flow analysis suggested increased resistance in the small vessels in chronic hypoxia and in larger vessels in diabetes. Fetal plasma nitrotyrosine levels, measured as a marker of peroxynitrite (reaction product of superoxide and nitric oxide), mirrored the differences in fetoplacental resistance, suggesting a causative role. Fetoplacental vasoconstrictor reactivity to acute hypoxic stimuli was reduced similarly in all groups. Fasudil, a strong vasodilator agent, reduced fetoplacental vascular resistance similarly in all groups, suggesting that for the observed differences among the groups, the changes in vascular morphology were more important than variances in vascular tone. Discussion: Maternal diabetes increases fetoplacental vascular resistance to a similar extent as chronic hypoxia. These stimuli are not additive. Changes in vascular tone are not responsible for these effects.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30105 - Physiology (including cytology)

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2018

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Placenta

  • ISSN

    0143-4004

  • e-ISSN

  • Volume of the periodical

    63

  • Issue of the periodical within the volume

    March

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    7

  • Pages from-to

    32-38

  • UT code for WoS article

    000426544800006

  • EID of the result in the Scopus database

    2-s2.0-85041420747